Viral load in HIV-associated dementia
Emory University, Atlanta, Georgia, United States Annals of Neurology
(Impact Factor: 9.98).
07/1998; 44(1):150-1. DOI: 10.1002/ana.410440131
Available from: Sergio de Almeida
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ABSTRACT: The pandemic of HIV/AIDS continues to grow daily. Incident cases among women, intravenous drug users and ethnic minorities comprise the fastest growing segment of the HIV-infected population, and the number of HIV-infected individuals over the age of 50 is growing rapidly. Today, the central nervous system and the immune system are seen as main targets of HIV infection. Significant progress in the knowledge and treatment of AIDS has been obtained in recent years. The neurological manifestations directly related to HIV are acute viral meningitis, chronic meningitis, HIV-associated dementia (HAD), vacuolar myelopathy, and involvement of the peripheral nervous system.
Brazilian Journal of Infectious Diseases 03/2006; 10(1):41-50. DOI:10.1590/S1413-86702006000100009 · 1.30 Impact Factor
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ABSTRACT: HIV encephalitis remains a prevalent and important neuropathological correlate of dementia in the HAART era. It is probably the only neuropathological variable that has undergone substantial independent verification in multiple autopsy cohorts. HIV encephalitis has provided the field with a unifying concept to pursue the pathophysiology of dementia. Drawbacks remain that the diagnosis is an overly diverse constellation of anomalies in both gray and white matter, and correlation with dementia remains too vague. The overall incidence of HIV-associated dementia in the HAART era declined by about half, but autopsy cohorts still exhibit a substantial prevalence of HIV encephalitis, probably because they are enriched with people with end-stage disease. The intensity of HIV encephalitis might have undergone a decrease in the HAART era, but HIV encephalitis remains essentially an "all or none" diagnosis. The criteria for a diagnosis of HIV encephalitis remain essentially intact but variants might have appeared in the HAART era. Examples include an increase in the number of cases with predominantly white matter necrosis ("leukoencephalopathy variant"), cases with only minimal or pathological change ("functional variant"), cases that have scars that lack evidence of HIV-1 after treatment with HAART ("burnt out variant"), cases with age-associated degeneration ("elderly variant") and cases in which immune reconstitution inflammatory syndrome has played a role ("inflammatory variant"). The partial disassociation between clinical dementia and HIV encephalitis remains a longstanding paradox of the neuro-AIDS field. It suggests that more than one underlying pathophysiological mechanism is present, and that co-morbid factors may be important. Progress in understanding the cliniconeuropathological correlation should advance because brain specimens collected under standardized conditions are available from the National NeuroAIDS Tissue Consortium. The incidences of opportunistic infection and tumors in the CNS underwent decreases after HAART. HAART prevents these processes from developing, but initiation of therapy when there is an ongoing pathological process can provoke immune reconstitution (immune reconstitution inflammatory syndrome) and an intense pathological response in the CNS that is potentially fatal. HIV/AIDS might exacerbate diseases of brain aging, and aging could worsen HIV-1-associated neurocognitive disability. The neurobiological interaction between persistent HIV-1 infection and brain aging remains unclear. Brain aging is universal to all populations, so neuropathological study in people with HIV/AIDS must control for chronological age. In the peripheral nervous system painful H-DSP is the most prevalent neurological problem of HIV/AIDS in the HAART era. The distal dying-back small fiber type of neuropathy still produces a disabling neuropathic pain. Measuring the loss of distal nerve fibers in the epidermis of a skin biopsy is a new diagnostic approach that is potentially useful to track disease progression and/or nerve regeneration experimentally. Even though the pathology occurs in the distal terminals, it remains likely that the driving force is a more proximal dorsal root ganglionopathy that is not characterized neuropathologically, or experimentally. Signs of HIV encephalitis and other opportunistic infection in the spinal cord have declined in the HAART era. The prevalence of HIV-associated vacuolar myelopathy has waned primarily because the lesion was predominantly observed in end-stage of AIDS, which is less prevalent. Gracile tract atrophy remains prevalent, and probably results from both sensory peripheral neuropathy and aging.
Handbook of Clinical Neurology 02/2007; 85:301-17. DOI:10.1016/S0072-9752(07)85018-4
Available from: Richard M. Ransohoff
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ABSTRACT: Chemotactic cytokines (chemokines) have been traditionally defined as small (10-14kDa) secreted leukocyte chemoattractants. However, chemokines and their cognate receptors are constitutively expressed in the central nervous system (CNS) where immune activities are under stringent control. Why and how the CNS uses the chemokine system to carry out its complex physiological functions has intrigued neurobiologists. Here, we focus on chemokine CXCL12 and its receptor CXCR4 that have been widely characterized in peripheral tissues and delineate their main functions in the CNS. Extensive evidence supports CXCL12 as a key regulator for early development of the CNS. CXCR4 signaling is required for the migration of neuronal precursors, axon guidance/pathfinding and maintenance of neural progenitor cells (NPCs). In the mature CNS, CXCL12 modulates neurotransmission, neurotoxicity and neuroglial interactions. Thus, chemokines represent an inherent system that helps establish and maintain CNS homeostasis. In addition, growing evidence implicates altered expression of CXCL12 and CXCR4 in the pathogenesis of CNS disorders such as HIV-associated encephalopathy, brain tumor, stroke and multiple sclerosis (MS), making them the plausible targets for future pharmacological intervention.
Progress in Neurobiology 03/2008; 84(2):116-31. DOI:10.1016/j.pneurobio.2007.11.003 · 9.99 Impact Factor
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